Astrocytes Mediate In Vivo Cholinergic-Induced Synaptic Plasticity

Abstract

In vivo and in vitro studies reveal that astrocytes, classically considered supportive cells for neurons, regulate synaptic plasticity in the mouse hippocampus and are directly involved in information storage.

Morphological plasticity of astroglia: Understanding synaptic microenvironment

“…A growing body of experimental evidence suggests that astrocyte signaling can, at least in certain conditions, influence excitatory synaptic transmission and its use‐dependent plasticity in a Ca 2+ ‐dependent manner (Henneberger et al, 2010; Jourdain et al, 2007; Min and Nevian, 2012; Navarrete et al, 2012; Parri et al, 2001; Perea and Araque, 2007). This does not necessarily imply that elegant experimental manipulations with astroglial Ca 2+ within a certain dynamic range by triggering certain cellular cascades should reproduce such effects (Agulhon et al, 2010; Fiacco et al, 2007; Petravicz et al, 2008) (see (Rusakov et al, 2014; Volterra et al, 2014) for discussion).…”

Functional MRI in Mice Lacking IP3-Dependent Calcium Signaling in Astrocytes

“…However, previous experiments using these animals have importantly showed a loss of Ca 2+ activity in astrocytic cell bodies and perivascular endfeet (both spontaneous activity and evoked by neuronal stimulation or pharmacological manipulations of G q -linked G-protein-coupled receptors) without any apparent compensation, and in the presence of an intact Ca 2+ activity in neurons. 9,13,14 Different cell types and physiologic and metabolic compartments have been proposed to contribute to the generation of functional hemodynamic responses. 2 Our results, however, do not discard the potential contribution of astrocytes to CBF regulation through different molecular mechanisms not requiring IP 3 R2-mediated Ca 2+ surges.…”

How Do Astrocytes Participate in Neural Plasticity?

“…Findings from three independent laboratories show that mice in which astrocytes cannot mobilize cytosolic Ca 2þ stores (IP 3 R 2 knockout mice) failed to develop long-term enhancement of excitatory transmission in response to combined stimulation of cholinergic and sensory inputs. In these studies, sensory input (whisker [Takata et al 2011], visual stimulation [Chen et al 2012], or tail pinch [Navarrete et al 2012]) in combination with stimulation of nucleus basalis or cholinergic fibers resulted in a sustained potentiation of excitatory transmission. Thus, emerging evidence suggests that neuromodulators may not only be responsible for spontaneous and evoked astrocytic Ca 2þ signaling in awake mice, but also for long-term neural plasticity .…”